Oliver's mTOR Atlas Evidence Platform
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Pathway link MTORC1-S6K1

mTORC1 S6K1

mTORC1 activates S6K1.

mTORC1 switches on S6K1, which turns on the cell's protein-building machinery – the classic effect most studies of this drug class measure.

mTORC1 phosphorylates S6K1, switching on the translation machinery. This is the classic rapamycin-sensitive output and the readout most papers actually measure.

The conditions it holds under

Caution: p-S6K is a proxy, not the phenotype. Many 'mTORC1 activity' claims rest on this single band.

Standard mTORC1 readout, but a readout is not the whole output. S6K1 phosphorylation is fully rapamycin-sensitive while 4E-BP1 is not, so 'mTORC1 activity' measured by S6K1 alone systematically overstates how much rapamycin inhibits mTORC1.

Time it takes
minutes
Step
direct (one molecule acts on the other)
Measured in
mammalian cells
Where in the cell
cytosol
Reaches people?
plausible in people, not shown directly
How settled
settled in the literature

Studies behind it

YearEvidenceStudy
1998 M RAFT1 phosphorylation of the translational regulators p70 S6 kinase and 4E-BP1BUR1998 RAFT1/mTOR directly phosphorylates p70 S6K (Thr389) and 4E-BP1, the two central translational effectors.
1992 M Rapamycin-FKBP specifically blocks growth-dependent activation of and signaling by the 70 kd S6 protein kinasesCHU1992 Rapamycin-FKBP12 complex blocks growth-factor activation of p70 S6 kinase, linking the drug to a specific mitogenic pathway.
2005 M mTOR and S6K1 mediate assembly of the translation preinitiation complex through dynamic protein interchange and ordered phosphorylation eventsHOL2005 mTOR and S6K1 dynamically assemble the translation preinitiation complex on eIF3.
2013 M mTORC1 phosphorylation sites encode their sensitivity to starvation and rapamycinKAN2013 Each mTORC1 phosphorylation site has its own intrinsic 'substrate quality'. Good substrates stay phosphorylated when mTORC1 is partly inhibited by rapamycin or starvation, poor ones drop out first, and changing a few residues around a site shifts its sensitivity in cells. One level of mTORC1 activity can therefore produce different output profiles.
1998 M Amino acid sufficiency and mTOR regulate p70 S6 kinase and eIF-4E BP1 through a common effector mechanismHAR1998 Amino acid sufficiency signals through mTOR to p70 S6K and 4E-BP1 via a common effector, first linking nutrients to mTOR.
2003 M The mammalian target of rapamycin (mTOR) partner, raptor, binds the mTOR substrates p70 S6 kinase and 4E-BP1 through their TOR signaling (TOS) motifNOJ2003 Raptor binds mTOR substrates via their TOS motifs, acting as the substrate-presenting scaffold of mTORC1.

Points the other way

No study in the Atlas contradicts this link. That means none in this curated set, not none in the literature.

Who has checked this

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Curator sign-off
Not signed off yet. This link was drafted with AI help and has not been reviewed link by link; treat it as a proposal until it is.
Curated by
Oliver Barton, with AI help for drafting; see how links are checked.

“How settled” describes how far researchers in the field agree. It is not the same as the sign-off above, which only says whether a named curator has checked this page.

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